Thursday, June 9, 2016

A Serious Challenge to the 2012 Low-carbohydrate "Metabolic Advantage" Study

Warning: this post will be a bit more wonkish than usual, because I need to get detailed to make my points. To read a summary, skip to the end.

In 2012, David Ludwig's group published an interesting RCT that suggested a substantial "metabolic advantage" resulting from a high-protein, very-low-carbohydrate diet (VLC) (1). In other words, this diet led to a higher energy expenditure relative to a normal-protein, low-fat diet (LF) over a one month period (a low-glycemic-load, normal-protein diet was in the middle and not significantly different from the other two). Resting energy expenditure (REE) was slightly but significantly higher on the VLC diet, and total energy expenditure (TEE) was elevated by a whopping 300+ kcal/day! I covered the study at the time, describing it as "fascinating" and "groundbreaking", and calling for the study to be replicated so we can be more confident in its unexpected result (2).

This finding has been used by Ludwig, Gary Taubes, and others to support the carbohydrate-insulin hypothesis of obesity, although there is no evidence that the effect was mediated by insulin, and also no evidence that it was mediated by reduced carbohydrate rather than increased protein (3).

Since I published that post, my confidence in the finding-- and particularly the common interpretation of it that reducing carbohydrate intake to a very low level increases REE and TEE-- has gradually been eroding. This is partially because other studies have generally reported that the carbohydrate:fat ratio of the diet has little or no effect on REE, TEE, or fat storage (4, 5, 6, 7, 8, 9, 10).

My confidence level dropped even more this week, when I saw a critical comment Kevin Hall added to the study in PubMed Commons (11). Ludwig and colleagues have since responded (12). Here's my perspective on the exchange, organized by topic:

Inconsistency between reported energy expenditure and weight change

Hall pointed out that measured TEE was ~200-500 kcal/day higher than reported energy intake for all diets, with the largest gap in the VLC diet. In other words, 200-500 more kilocalories were going out than were going in. Over a four-week period, if the data are correct, the VLC diet should have caused just over a kilogram of weight loss-- but it didn't-- the VLC diet group actually gained a small amount of weight (0.5 kg). This internal inconsistency in the data may suggest that one or more of their measures is incorrect, either body weight (unlikely), energy intake (likely, as explained below), and/or energy expenditure (possible, as explained below).

Ludwig responded that body weight is an unreliable measure of energy balance over short periods of time-- in other words, there could have been differential changes in body composition between groups that masked a body weight loss effect. I do agree that small changes in body weight over short periods of time aren't a very solid measure of energy balance, but what Ludwig is proposing here is basically that the VLC group was gaining water weight and/or lean mass to offset fat loss that was simultaneously occurring. This hypothesized water/lean mas gain would have to offset more than 1.5 kg of weight change (just over 1 kg predicted from TEE, + 0.5 kg weight gain on VLC diet). Since we know that VLC diets tend to reduce water weight, and are unlikely to pack on 1.5+ kg of lean mass in a month (particularly in the face of a diet that does not meet energy needs), Ludwig's explanation is hard to believe.

This brings us to what is probably the real reason for the lack of change in weight.

Incomplete diet adherence

When I first wrote about this study, I don't think I fully appreciated the likelihood that the volunteers would "cheat" and eat outside food. Ludwig's team provided them with all study foods, but since it wasn't a metabolic ward study, volunteers had the ability to eat additional food at home. I'll add that these people had a strong incentive to eat more, because they were maintaining a 10-15% reduced body weight throughout the study. This means they were hungry and highly motivated to eat additional food at home.

And they probably did. This may explain the fact that the volunteers gained a bit of weight on all diets, despite the fact that their supposed energy intake was hundreds of kilocalories lower than their energy expenditure! Ludwig acknowledges this in his comment, saying "it is likely that some non-study foods were consumed". He downplays it, but we're talking about 200-500+ kcal/day here, which is not insignificant.

I understand that this kind of study is challenging to do, and the design is certainly a lot more rigorous than the type of diet study where you just send people home with diet advice and let them cook their own food. This type of study design works well in a lot of contexts, but perhaps it isn't the best suited for situations where your volunteers are weight-reduced and have a strong incentive to eat additional food.

Statistical weaknesses

The study declared REE as the primary outcome, and it found that the VLC diet had a significantly higher REE than the LF diet. The difference was only 67 kcal/day, but this finding is robust because it was declared in advance as the primary outcome. I think we can be fairly confident that, under the conditions tested, the VLC diet led to an increase in REE vs. the LF diet. However, the increase is small enough that it has little clinical or practical significance.

But the big splash made by this study wasn't the 67 kcal/day increase in REE-- it was the ~300 kcal/day increase in TEE! Although this finding got all the press, it rests on much less solid ground, as pointed out by Hall. The reason is that it's one of many secondary outcomes (66 possible statistical tests performed on 22 measured variables, to be exact), and when you have so many possible outcomes, you end up with a high likelihood of a false positive finding unless you use specific statistical tools to correct the problem. This is called the multiple comparisons problem and it's very common in science. In fact, it's one of the leading causes of unreliable findings in the scientific literature.

As I said, the multiple comparisons problem can be avoided by using the right statistical tools (essentially, raising the bar for statistical significance in proportion to the number of statistical tests you perform), but in Ludwig's study, these tools were not sufficiently applied to give us confidence in the secondary outcomes. And that's not actually as bad as it sounds, but it does necessitate an additional layer of interpretation. Basically, if you don't adequately correct for multiple comparisons, your finding is "exploratory"-- meaning it's not a statistically robust finding, but it is suggestive and can be used to guide further research. Researchers do this all the time, and in my opinion it's acceptable as long as it's clearly labeled as exploratory. But it also means that you can't (or shouldn't) proclaim to the public that a diet increases TEE by hundreds of kilocalories per day, because that result is not statistically robust.

So to summarize, we're left with a small REE effect that is statistically robust, and a large TEE effect that is statistically questionable. And as we will see, the REE effect is likely explained by the higher protein content of the VLC diet.

The confounding effect of protein

The VLC diet was 30% protein by calories, while the other two diets were 20% protein. Since high-protein diets are known to increase energy expenditure, this may provide a plausible explanation for the observed increase in REE on the VLC diet.

In Ludwig's response to Hall's critique, Ludwig states that the higher protein content of the VLC diet can't explain the higher REE: "A protein difference of this magnitude can’t explain differences in REE in the fasting state, long after the thermic effects of food have dissipated". But in fact, other RCTs demonstrate that it can explain the increase in REE.

In 2013, the research group of Margriet Westerterp-Plantenga at Maastricht University-- one of the leading researchers in this area-- published a study that examined the effects of high-protein vs. normal-protein diets on REE after weight loss (13). It's worth noting that protein was increased at the expense of fat, not carbohydrate.

Following a weight loss of about 7 kg in both groups, the normal-protein group experienced a reduction of REE, but the high-protein group didn't. The between-group difference in REE during weight maintenance? 81 kcal/day. This is very similar to the 67 kcal/day that Ludwig reported, except that it was produced by increasing protein alone, not a combination of high protein and very low carbohydrate as in Ludwig's study. In my view, high protein intake probably explains the elevated REE in the VLC diet group.

Summary
The 2012 study by David Ludwig's group reported that in subjects maintaining weight loss, a high-protein, very-low-carbohydrate diet increased resting energy expenditure by a small amount (67 kcal/day), and total energy expenditure by a large amount (~300 kcal/day), relative to a normal-protein, low-fat diet. Superficially, this seems to support the idea of a substantial "metabolic advantage" for very-low-carbohydrate diets. However, there are reasons to be skeptical of some of the findings, which Kevin Hall laid out in a comment on NIH Commons. Here's a summary of my current views:

There was probably significant dietary non-compliance, with volunteers eating extra food at home in addition to what they were supplied by the lab. This probably explains at least part of why they didn't lose weight, despite the fact that they should have lost weight according to the reported energy intake and expenditure figures.

The finding that resting energy expenditure was elevated on the VLC diet is statistically robust. However, the increase is small enough that it has little clinical or practical significance.

The increase in resting energy expenditure can be explained by the higher protein content of the VLC diet, and it probably had little to do with the fact that the VLC diet was low in carbohydrate.

The finding that total energy expenditure was elevated by ~300 kcal/day on the VLC diet is not statistically robust, and it's also hard to reconcile with the results of other studies.

For me, here's the bottom line. Aspects of the study still stand as reliable, but the findings do not support the conclusion that reducing carbohydrate intake yields a metabolic advantage. My best interpretation is that the study is consistent with other findings suggesting that high-protein diets yield a small metabolic advantage, but that calorie intake is still the key determinant of fat mass changes.

Normalcarb, did you read Stephan's comments that it was probably not the carb intake that made the difference but the higher protein intake? The evidence for lower carb intake equalling weight loss just isn't there in this study or any others.

normalcarb said..."If you believe that most people gain about 1 lb a year on average, wouldn't that small advantage become HUGE over the long term? Assuming, of course, that they adopted VLC as a lifestyle."No. As Energy Expenditure decreases with decreasing weight, a change in Energy Intake of 100 kcals/day leads to a long-term change in weight of 10 lbs. Ref: A Mathematical Challenge to Obesity

Therefore, a change in Energy Intake of 67 kcals/day leads to a long-term change in weight of 6.7 lbs.

> Warning: this post will be a bit more wonkish than usual, because I need to get detailed to make my points. To read a summary, skip to the end.

Personally, I started following Whole Health Source because of the wonkish posts, so I appreciate the return to form!

> As I said, the multiple comparisons problem can be avoided by using the right statistical tools (essentially, raising the bar for statistical significance in proportion to the number of statistical tests you perform), but in Ludwig's study, these tools were not sufficiently applied to give us confidence in the secondary outcomes.

Actually, I think that even trying to correct for multiple comparisons is now considered inadequate by many, because of the garden of forking paths problem. Andrew Gelman has some posts on this on his blog if people are interested, I believe.

Just some quick thoughts / questions :- why do we call it a metabolic "advantage" ? We should stay objective and call it an increase in metabolic rate (MR)- what can possibly cause this increase ? In a VLC context of short duration, you still need glucose (as opposed to long term VLC'ing where ketone bodies can partially compensate). So if you provide an increase amount of dietary protein, some will be broken down for manufacturing glucose, eventually. I suspect it is more costly from a energetic POV than ingesting carbs for glucose.

So my impression is that whatever slight increase in MR in VLC diet is due to protein use for glucose, not necessarily more body fat oxidation, which any VLC'er tends to believe they achieve by stuffing themselves with fatty foods sans carbs.

A 67 kcal change in population energy balance would go about 1/3 of the way toward reversing the US "obesity epidemic" (which was produced by a ~218 kcal/day increase in energy intake), so yes, it would be quite significant. But there are much easier ways to burn an extra 67 kcal/day than a high-protein, VLC diet! That works out to about 10 minutes of jogging per day, or a 1-mile walk (most semi-sedentary people walk ~2.5 miles/day just doing normal everyday activities). Or, on the other side of the energy balance equation, cutting your calorie intake by 2/3 of a slice of toast per day.

And as others have said, the very-low-carbohydrate portion of the intervention appears to be superfluous to the effect on energy expenditure. That said, it may not be superfluous for changes in energy intake. In other words, there is evidence that VLC reduces calorie intake-- so there is still some basis for it being an effective weight loss tool.

Hi Nigel,

Your math is correct, but since the average population weight gain that has produced the obesity epidemic is on the order of 20 lbs per person (with that burden of course unevenly distributed among individuals), an average reduction of 6.7 pounds is still pretty significant on a population level.

Hi BJ Terry,

Thanks for that-- I'll read it. I'm not currently aware of that issue, but my stats knowledge is pretty basic.

Hi Thorgal,

I agree with your point about the term "metabolic advantage". I wouldn't use that term in a scientific paper. The reason I use it here is that it's concise and easy to understand for a more general audience.

Regarding the explanation for the protein-induced increase in energy expenditure, this is something that has been researched by several investigators. The two explanations that I find the most compelling are 1) amino acids act directly on brain energy balance circuits to dampen the adaptive metabolic "starvation response" to weight loss, and 2) higher protein helps preserve lean mass in the face of a calorie shortfall. Klaas Westerterp and Margriet Westerterp-Plantenga have written extensively about this.

@nigel, there is some protein catabolism during the transition to a VLC diet. It's been documented by Stephen Phinney to start at around 25g in the first day and to taper off to zero after about 3 weeks.

So, assuming 25g is the peak, and that the protein is being converted to glucose via GNG at 67% efficiency, we can estimate the peak increase in RMR due to that protein catabolism at around 33 kcal. Hall saw a much higher peak than that, so it probably wasn't just due to protein.

So what's the source of the chronic increase increase in RMR? My guess is that it represents the cost of ketogenesis. Ketones can supply about 2/3's of the brain's energy requirements on a VLC diet. Those ketones aren't free. Hall himself estimates the cost as around 20% (in a communication to Peter Attia).

The brain uses about 500 kcal/day.

2/3's supplied by ketones = 333 kcal/day.

If the cost is 20%, then we'd need 67 kcal/day extra to supply that 333 kcal/day of ketones.

As a career industrial researcher, sorting out the significant effects in multifactorial experiments was matter-of-course. I lost pride of ownership for my own ideas pretty early in my career. My foolish ideas made good conversation starters with real-life observers though, and resulted in better experimental designs going forward.

With the HFLC (or vegan, or fruitarian, or cleasers, pick any of them) nutritional warriors I don't see normal rational discussions. They're unwilling to compile lists of factors, then subject them to simple screens like Pareto analysis, and move on to verification. This shouldn't take any longer than a few months. They're modern flat earth fraternities, which don't subject their simplistic single factor viewpoints to verification.

I adopted a term for this behavior, which one of my technicians used in another context. Flogging. The worst floggers were researchers who had the ability to get grant money based on their tenure/prestige. I remember one academic researcher who had the ability to get Canadian government grant money for his endless studies. His work was meticulous and always impressed me when I read it in journals. At a conference I discussed one of his presentations with some Canadian industrial researchers, who commented "At least you don't have to pay for it". After that I paid closer attention to my own work...

@normalcarb interesting. 25 grams a day of dry protein loss from muscle wastage during ketosis dieting? That represents half a pound a day of muscle weight, and even with the taper-off over 3 weeks would represent 5 pounds of muscle lost. It was hard to preserve muscle mass when I was losing weight at a 10 pound per month rate. I blame a snapped rotator cuff tendon (supraspinatus) on the resulting weakness in my shoulders. It appears that ketosis dieting would have been far worse, and I'm glad I didn't go that way.

normalcarb said..."@nigel, there is some protein catabolism during the transition to a VLC diet. It's been documented by Stephen Phinney to start at around 25g in the first day and to taper off to zero after about 3 weeks."Link us to the document, as 25g/day is way too low.

According to Liver and Kidneys Synthesize Glucose, hepatic glucose production from amino acids peaks at ~50g/day from amino acids, and renal glucose production peaks some time later at ~30g/day from amino acids. Conversion of protein to glucose is ~50% efficiency (not 67%), so protein catabolism peaks at ~100g/day for the liver and ~60g/day some time later for the kidneys.

Your assumptions and the rest of your maths are therefore invalid, apart from "The brain uses about 500 kcal/day." which is about right.

"2/3's supplied by ketones" is incorrect. Scroll down to "Circulating Nutrients in Starvation.""After about 2 weeks of adaptation, about 50% of the brain's energy comes from glucose, and the remaining 50% from oxidation of ketone bodies."

"Interesting that my estimates matches Ludwig's results, eh? :)"When you pull numbers out of thin air, I'm not surprised that you arrive at the desired result.

Arguing about which foods/macronutrients/micronutrients cause obesity is pointless, as foods/macronutrients/micronutrients aren't responsible for causing obesity.

Refined sugar & ultra-fine flour were invented in ~1880 and Americans ate more carbohydrate from 1909 to 1929 than they do now (graphs elsewhere on Stephan's blog), yet BMI in the US began to increase slowly after ~1945, according to https://pbs.twimg.com/media/CjzW6c3UkAIxkVu.jpg:large. How come?

BMI started to increase rapidly after 1990, ~10 years after the so-called fattening guidelines were released (guidelines which weren't followed, by the way). How come?

While this debate does not pertain directly to muscle loss, it includes a reanalysis of Phinney's 1983 bicyclist study which claimed no loss in performance among keto riders. Aragon picks up on Phinney's statement that sprint performance was deteriorated in the keto riders. And to Stephan's point above, Aragon also picks up on the problems with statistics in that study of 5 riders:

"However, the authors’ conclusion is misleading since 2 of the 5 subjects experienced substantial drops in endurance capacity (48 & 51-minute declines in TTE, to be exact). One of the subjects had a freakishly high 84-minute increase in TTE, while the other increases were 3 & 30 minutes. The outlying high value was instrumental in skewing the results away from any significant decline in the keto condition’s mean TTE."

An honest scientist would throw out the outlier, especially an outlier so extreme that it determines the study's no-effect conclusion.

In this study Davis and Phinney note that muscle loss is indicated in ketosis weight loss diets with insufficient protein due to loss in VO2 max, but does not give grams muscle loss.

http://www.ncbi.nlm.nih.gov/pubmed/2104036

I recall reading of a .25 lb loss in muscle mass in the first 3-4 days of one of Phinney's ketosis studies on trained athletes, but cannot locate that study.

Here's the Phinney reference on lean weight loss at .25 lb in 3-4 days. It's also noted that the riders were eating 1.7 grams of protein per kg body weight. Weight loss dieters (such as myself) who don't dramatically increase their protein consumption would suffer much more muscle atrophy/lean mass wasting than the riders. In a reduced calorie weight loss diet 45% protein/35% carb/20% fat would be a good target IMO. That's a LOT of tuna and tofu.

The very serious problem with the Ludwig/Phinney/Volek elevated protein methodology is that it only makes sense on a high calorie diet for athletes. For an obese 100 kg person eating 1500 calories a day for weight loss, the protein level needed to preserve lean mass consumes a very significant part of daily calories. Using Phinney's 1.7 g protein/kg cyclist, it's 170 grams a day - 10 cans of tuna - 45% of daily calories on a 1500 calorie per day diet.

Eating that much tuna would be a challenge for most people. I can't imagine how someone would do this on a primarily vegetarian diet.

Very interesting. Two tangential questions: what do you use to stay abreast of these PubMed comments--do you choose papers or topics that it will send alerts on? And why don't you reply with your thoughts that you wrote here? Or do you feel Hall addressed then enough? I guess he'd have dibs on any rejoinder.

While correlations do not show causation - this warrants better studies. One place claims a 200 day half life of LA in adipose tissue - thus cause and effect are distant and less noticed by people.

Some oils were being added to foods after the war - rations that didn't spoil etc. Even in 1960 - 1965 few people were packing much weight. It was in about 1960 that the push to market vegetable oils really took off.

My hunch is the effect of LA on mitochondria and insulin sensitivity is the real problem. Once people get overweight, they become insulin resistant (as they should - they need to be resistant to lose the excess weight) and the system breaks.

You can't look at insulin by itself - only with the backdrop of sensitivity will it make sense. The receptors sensitivity is just as important as the signal. We know that LA effects insulin sensitivity.

Uncontrolled studies like this are not likely to give us the answers we quest for. ( We need synthetic diets on controlled subjects (prison populations? ).

My hunch ( anyone on either side of the argument that says they know for sure, clearly does not understanding the question) is that eating low-carb can compensate for the effects of a high LA diet to some extent.

In terms of the brain's utilization of ketones, see Cahill and Owen's famous study:http://www.ncbi.nlm.nih.gov/pmc/articles/PMC292907/

In any case, we're talking about a relatively small increase in REE due to these metabolic changes. The TEE changes are potentially more interesting. A lot of people report feeling an increased "energy" on VLC, even a mild euphoria, but obviously there's a lot more variation in TEE.

More interesting to me is the effect on appetite, and I'm hoping Hall says something about that when his study is published. He alluded to "interesting" appetite effects in his interview.

Another problem with the Phinney/Volek/Lustig approach is the cost of protein vs fat or carbs. 8 cans of tuna a day is $10 (and at least $50 if you did it on fresh wild fish or reindeer the Paleo way). 4 tubs of cottage cheese about $10. This is protein equivalent to 6 - 14 oz tofu packs which cost about $15. The cheapest option of all would probably be eating half a bag of Bob's gluten or TVP at $5. For an aggressive 6 month weight loss plan to lose 50 lbs you could mix them up to enhance your daily enjoyment. Or you could just buy the 1600 cans of tuna or 80 sacks of TVP at Costco right up front, move into your man-cave, and do it right.

The new high protein approach to dieting makes old-style Atkins look like a smorgasboard.

Those graphs don't explain why BMI is low and stable until 1945, then increases, then stabilises from ~1965 to 1990, then rapidly increases after 1990.

Here's an alternative explanation:-After World War 2, the economy was in a slump and something had to be done to get people to buy more stuff, to stimulate economic growth. Corporations changed the way that they marketed to people. Instead of appealing to people’s logic, they began to appeal to people’s emotions. It worked.

One of Bernays' dirty tricks is confusing the public by promulgating conflicting information. The Tobacco Industry paid health professionals to advertise cigarettes. On the one hand, you had researchers telling people that smoking was bad for them and on the other hand you had a doctor on TV saying that he preferred to smoke Camel cigarettes. This confused the public and made them mistrust researchers & science. Another dirty trick was setting-up organisations with scientific-sounding names to promulgate conflicting reports which the press published as “science”, saying that “X” was good for you, then some time later “X” was bad for you, then some time later “X” was good for you again and so on. The public mistrusted researchers & science even more.

The recent NOF report from Malhotra et al telling people to eat more fat is conflicting information, resulting in even more public confusion and even more mistrust of researchers & science. This is exactly what the Food Product Industry wants.

@nigel @karl increasing LA is what salty snack foods are all about. The LA is critical for increasing our appetite for them. Yet no one is on a soapbox about limiting the size of salty snack food portions. Paleo/HFLC deflects attention away from fat to fructose, which is not a major issue. Bloomburg deflects attention away from fat to limiting the size of sodas. Yet every day I walk by the empty mylar chip bags...not many empty soda cups....

80% of the 500 calorie increase in consumption USDA documents 1970-2005 is refined grains (glucose from potato and corn starches) and added fats (high LA vegetable oils like corn and soy). About equal amounts of each. USDA 2010 diet data shows that 43% of our dietary calories now come from fat. Malhotra wants us to eat more?????? How much do they have to ram down our throats before they're satisfied?

thhq said..."@nigel @karl increasing LA is what salty snack foods are all about. The LA is critical for increasing our appetite for them."That may well be true, but in the graph from Vegetable Oil and Weight Gain, US pufa consumption increased rapidly from 1999. BMI increased rapidly from 1990, when pufa consumption was fairly constant, so pufa consumption wasn't the cause.

That is exactly what one would expect. Glucose is oxidized by tissues based on availability, and it displaces fat oxidation. So the more glucose you have in your bloodstream at any given time, the more glucose your body burns, and the less fat. High-glycemic carbs create greater glucose availability immediately after the meal, displacing fat oxidation to a greater degree. Low-glycemic carbs have a delayed availability but the glucose still shows up in the bloodstream eventually. If both conditions contain the same amount of carbohydrate, the body ends up burning the same amount of carbohydrate and fat over a 24-hour period, it's just that the timing is different because glucose levels are elevated on different trajectories.

This has no implications for body fatness because at the end of the day, the same amount of carbohydrate and fat end up being consumed. The only way low-glycemic carbs could impact body fatness is if they get you to eat fewer total calories or if they increase total calorie expenditure.

@Stephan Sorry - but I'm not following your narrative. Janus said that there is more fat oxidized - you are saying " the body ends up burning the same amount of carbohydrate and fat over a 24-hour period, " I think you mean something other than what it sounds like you mean?

I would expect that 'more fats are oxidized' (very small change) to be true due because our bodies adaption to exposure to high levels of carbs (unless you think all of Phinney's papers are wrong?) - this study had periods of only 3-days (I'm not impressed by the design - we need to be doing synthetic diets - under real controlled conditions (people tend to cheat) for longer periods). 3-days is enough to start having an effect if the peak exposure to carbs matters (I'm doubt the effect is linear - but don't think we know).

That being said - I'm not impressed by low GI diets as not only does the area under the curve matter - but low GI diets are digested so slowly, that they interfere with the induction of insulin resistance during sleep in the morning hours (needed to lose weight). A meal high in complex carbs at bed time can prevent reaching the normal ketosis by morning.

Somewhat higher BG all the time vs spikes might have some advantage for other disease processes - several bits become toxic only when BG is over a certain threshold. We don't want to forget this paper - I remember but can't find another paper that had to do with iron overload vs BG. Even postprandial BG spikes over 110 increase processes that are probably not healthy. ( fit children - fit adults - my father when he was 88 (not over weight (avoided deep-fried food) will maintain BG under 110. The limit I've seen in the medical community of 140 produces cognitive dissonance and makes my head hurt. Seems to be based on averages - not health.)

Now if someone gets overweight - it appears one symptom is that the body responds by losing insulin sensitivity (which should produce weight loss). If the medical community responds by giving meds to lower BG (instead of diets), weight loss becomes difficult or impossible. Eating diets high in PUFA (particularly LA) will reduce BG - but apparently at the expense of maintaining or increasing obesity. If the 600-day half life of LA in adipocytes is true - cause and effect are greatly separated in time - reducing the likely-hood that the public will realize what is keeping them overweight (as they eat their LA soaked salads)

On a low carb (not low GI) diet long term, we lose the ability to deal with high carbohydrate meals to some extent (probably a lot of personal variation) - it is apparently important to get some exposure to carbs or you can get to the place where even moderate protein consumption can raise BG. These adaptions take time - perhaps a 'time constant' of a week? But if someone is switched to a low-GI diet - it could effect these adaptions a small amount short term.

The paper does the usual thinking of changes in insulin levels in the absence of considering changing insulin sensitivity ( which varies quite a bit over the course of a day). With out realizing that sensitivity + level are inputs to the same control loop, understanding remains out of grasp.

Stephan, I totally agree with needing to eat less calories - calories in - calories out = the delta of body weight. Our bodies evolved appetite regulation eating quite different foods than the high carb + plus VERY high PUFA diets of today.

The lines waver from year to year, but if you lay a straightedge through PUFA and MUFA both are uptrending from 1970-2000. MUFA has a stronger uptrend through the 1990's, and represents the largest single contribution to total fat consumed. According to the USDA analysis this represents increasing use of higher MUFA vegetable oils such as olive and canola for salads and frying. The MUFA contribution from meats, poultry and fish has been steadily declining.

So while PUFA consumption is flat in the 1990's it does not indicate any flattening in overall vegetable fat consumption, just a shift in the type of vegetable fat.

Slightly off topic, but an N=1 experiment in progress is that of Andrew Taylor, or " spud fit" he is on day 180 ish of a full year just eating potatoes.....thus far he has lost 90+ pounds, or 0.5lb per day! Eating approximately 3.5kg of spuds per day. A case in point of 90% plus CHO diet with extremely low reward.

Look at it this way. The study Janus cited measured CHO oxidation shortly after a meal. It didn't measure 24 hr CHO oxidation. If you eat low-glycemic carbs, you oxidize less CHO now and more later because the blood glucose curve is shifted. 24-hr CHO oxidation remains the same.

This has to be the case, because the body has a very limited ability to store CHO, and the storage space can't expand infinitely like body fat. What this means is that in the long run, you oxidize exactly the same amount of CHO you ingest, whether that CHO is high or low glycemic. It is literally physically impossible to oxidize less CHO than you consume over a prolonged period of time, unless you're diabetic and you're pissing it out, simply because the body is incapable of accumulating CHO so intake always equals oxidation.

Hi Stephan. I would be very interested in your views concerning the recently published results of research by Samantaha Solon Biets into carb protein ratios. These would seems to line up very much with your ideas concerning protein's value for younger people in reproductive years but not for post 50-y-olds where longevity is the goal.

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